scholarly journals Mechanisms of development of alcohol-dependant osteoporosis

2012 ◽  
Vol 93 (1) ◽  
pp. 120-122
Author(s):  
D N Goryachev ◽  
L R Mukhamedzhanova
Keyword(s):  
Mutual Influence ◽  
Organic Matrix ◽  
Collagen Type I ◽  
Published Data ◽  
Type I ◽  
Characteristic Features ◽  
Chronic Ethanol Intoxication ◽  
Immune Pathology ◽  
Mechanisms Of Development

Presented were the current published data on the mutual influence of different factors on the initiation and progression of disorders of formation of the bone organic matrix and its mineralization during chronic ethanol intoxication. Emphasized was the role of the toxic effect of ethanol on the osteoblastic cells, which is expressed in the increasing viscosity of the cytoplasm, disruption of the architectonics of the cytoplasmic membrane, disorganization of the polyribosomal complexes and reduction of the collagen synthesis functions. Established was the role of immune pathology, which included the formation of antibodies to a number of autogenous tissues. Found were antibodies to collagen type I, which was modified by acetaldehyde and possessed cytotoxicity. In patients with alcohol dependence noted was an increase in the concentration of interleukin-6, which stimulates the early stages of hematopoiesis and osteoclastogenesis. The mechanism of development of alcohol-dependant osteoporosis is understood as a cascade of related processes, which are linked in the circulus vitiosus. Only the initial stages of this cascade have certain specificity. The morphological consequences are mostly similar and do not differ from those of other forms of secondary systemic osteoporosis, however give the characteristic features to the clinical course.

scholarly journals WNT-5A regulates TGF-β-related activities in liver fibrosis

2017 ◽  
Vol 312 (3) ◽  
pp. G219-G227 ◽  
Author(s):  
Leonie Beljaars ◽  
Sara Daliri ◽  
Christa Dijkhuizen ◽  
Klaas Poelstra ◽  
Reinoud Gosens
Keyword(s):  
Liver Fibrosis ◽  
Functional Role ◽  
Collagen Type ◽  
Collagen Type I ◽  
Matrix Proteins ◽  
Type I ◽  
Human Livers

WNT-5A is a secreted growth factor that belongs to the noncanonical members of the Wingless-related MMTV-integration family. Previous studies pointed to a connection between WNT-5A and the fibrogenic factor TGF-β warranting further studies into the functional role of WNT-5A in liver fibrosis. Therefore, we studied WNT-5A expressions in mouse and human fibrotic livers and examined the relation between WNT-5A and various fibrosis-associated growth factors, cytokines, and extracellular matrix proteins. WNT-5A gene and protein expressions were significantly increased in fibrotic mouse and human livers compared with healthy livers. Regression or therapeutic intervention in mice resulted in decreased hepatic WNT-5A levels paralleled by lower collagen levels. Immunohistochemical analysis showed WNT-5A staining in fibrotic septa colocalizing with desmin staining indicating WNT-5A expression in myofibroblasts. In vitro studies confirmed WNT-5A expression in this cell type and showed that TGF-β significantly enhanced WNT-5A expression in contrast to PDGF-BB and proinflammatory cytokines IL-1β and TNF-α. Additionally, TGF-β induces the expression of the WNT receptors FZD2 and FZD8. After silencing of WNT-5A, reduced levels of collagen type I, vimentin, and fibronectin in TGF-β-stimulated myofibroblasts were measured compared with nonsilencing siRNA-treated controls. Interestingly, the antifibrotic cytokine IFNγ suppressed WNT-5A in vitro and in vivo. IFNγ-treated fibrotic mice showed significantly less WNT-5A expression compared with untreated fibrotic mice. In conclusion, WNT-5A paralleled collagen I levels in fibrotic mouse and human livers. WNT-5A expression in myofibroblasts is induced by the profibrotic factor TGF-β and plays an important role in TGF-β-induced regulation of fibrotic matrix proteins, whereas its expression can be reversed upon treatment, both in vitro and in vivo. NEW & NOTEWORTHY This study describes the localization and functional role of WNT-5A in human and mouse fibrotic livers. Hepatic WNT-5A expression parallels collagen type I expression. In vivo and in vitro, the myofibroblasts were identified as the key hepatic cells producing WNT-5A. WNT-5A is under control of TGF-β and its activities are primarily profibrotic.

Role of catechin on collagen type I stability upon oxidation: a NMR approach

2019 ◽  
Vol 34 (1) ◽  
pp. 53-62 ◽  
Author(s):  
Massimo Lucarini ◽  
Fabio Sciubba ◽  
Donatella Capitani ◽  
Maria Enrica Di Cocco ◽  
Laura D’Evoli ◽  
...  
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Type I

Multiphoton Microscopy for Caries Detection with ICDAS Classification

2018 ◽  
Vol 52 (5) ◽  
pp. 359-366 ◽  
Author(s):  
Amel Slimani ◽  
Delphine Tardivo ◽  
Ivan V. Panayotov ◽  
Bernard Levallois ◽  
Csilla Gergely ◽  
...  
Keyword(s):  
Nonlinear Optical ◽  
Second Harmonic ◽  
Multiphoton Microscopy ◽  
Organic Matrix ◽  
Collagen Type I ◽  
Assessment System ◽  
Caries Detection ◽  
Major Protein ◽  
Type I ◽  
Carious Lesion

Dentin carious lesion is a dynamic process that involves demineralization and collagen denaturation. Collagen type I is the major protein in dentin and it has been investigated based on its optical properties. Multiphoton microscopy (MPM) is a nonlinear imaging technique that reveals the caries process using the collagen two-photon excitation fluorescence (2PEF) and its second-harmonic generation (SHG). Combining the histological and the International Caries Detection and Assessment System (ICDAS) classifications with nonlinear optical spectroscopy (NLOS), 2PEF and SHG intensities of enamel and dentin were highly altered during the caries process. It has been proven that the ratio SHG/2PEF is a relevant indicator of the organic matrix denaturation [Terrer et al.: J Dent Res 2016; 96: 574–579]. In the present study, a series of measurable signals is made to detect early stages of carious lesion according to the ICDAS classification and to explore the relationship between these measures and the ICDAS scale. Comparison of the efficiency of nonlinear optical signals for caries detection with the ICDAS classification is essential to evaluate their potential for clinical application. In our study, the use of the NLOS measured by MPM allowed us to monitor a quantitative parameter (SHG/2PEF ratio) according to the dentin carious lesion state (ICDAS and histological examination). Three coherent new groups were defined (ICDAS 0/1; ICDAS 2/3; ICDAS 4/5/6), where the carious process can be clearly described with a statistically significant decrease of the SHG/2PEF ratio.

Blockade of hypoxia-reoxygenation-mediated collagen type I expression and MMP activity by overexpression of TGF-β1delivered by AAV in mouse cardiomyocytes

2007 ◽  
Vol 293 (3) ◽  
pp. H1833-H1838 ◽  
Author(s):  
Chang-Ping Hu ◽  
Abhijit Dandapat ◽  
Yong Liu ◽  
Paul L. Hermonat ◽  
Jawahar L. Mehta
Keyword(s):  
Cardiac Remodeling ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Type I ◽  
Antioxidant Mechanism ◽  
Multifunctional Peptides ◽  
Expression And Activity ◽  
Hypoxia Reoxygenation

Transforming growth factor (TGF)-β1is one of the most pleiotropic and multifunctional peptides known. While the cardioprotective effect of TGF-β1during ischemia is well known, the specific role of TGF-β1in altering the cardiac remodeling process remains unclear. This study was designed to examine the regulation of hypoxia-reoxygenation-mediated collagen type I expression and activity of matrix metalloproteinases (MMPs) by overexpression of TGF-β1in cultured HL-1 mouse cardiomyocytes. TGF-β1was overexpressed in cardiomyocytes by transfection with adeno-associated virus (AAV)/TGF-β1Latentor with AAV/TGF-β1ACT(active TGF-β1). Twenty-four hours of hypoxia followed by 3 h of reoxygenation (H-R) markedly enhanced (pro)collagen type I expression and activity of MMPs concomitant with an increase in reactive oxygen species (ROS) release and LOX-1 expression. Overexpression of TGF-β1reduced these alterations induced by H-R. TGF-β1overexpression also blocked H-R-mediated p38 and p44/42 MAPK activation. Transfection with AAV/TGF-β1ACTwas superior to that with AAV/TGF-β1Latent. These data for the first time demonstrate that H-R induces signals for cardiac remodeling in cardiomyocytes and TGF-β1can modulate, possibly via antioxidant mechanism, these signals. These findings contribute to further understanding of the role of TGF-β1in the cardiac remodeling process.

The role of collagen type I α2 polymorphisms: intracranial aneurysms in Koreans

2009 ◽  
Vol 72 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Sung-Pil Joo ◽  
Tae-Sun Kim ◽  
Il-Kwon Lee ◽  
Jung-Kil Lee ◽  
Bo-Ra Seo ◽  
...  
Keyword(s):  
Intracranial Aneurysms ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I

scholarly journals Mining for the association of bovine mastitis linked genes to pathological signatures and Pathways

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Muhammad Zahoor Khan ◽  
Saadet Belhan ◽  
Nebi Cetin ◽  
Adnan Ayan ◽  
Adnan Khan ◽  
...  
Keyword(s):  
Influenza A ◽  
Prion Diseases ◽  
Bovine Mastitis ◽  
Venn Diagram ◽  
Published Data ◽  
Type I ◽  
Bioinformatics Tools ◽  
Common Infectious Disease ◽  
The Status

Abstract Background: Bovine mastitis is a common infectious disease with a serious threat to the dairy industry and public health. Mastitis is a polygenetic trait under the control of many genes. In the current study, our research attempted to address the role of mastitis-associated genes in various signalings including parasitic, viral, cancer and fungal diseases by using online bioinformatics software. Methods: We selected mastitis-associated genes from already published data and using online bioinformatics tools including DAVID and String classify the pathological role of relevant genes. A Venn diagram was used to show the status of overlapping genes among different biological function processes. Result: This study revealed that the genes gathered in published resources of mastitis were significantly correlated with Influenza A, Chagas disease, Leishmaniasis, Toxoplasmosis, Tuberculosis, Cancer signaling, Hepatitis B, Type I &II diabetes mellitus and Prion diseases biological pathways. Based on our findings, we concluded that mastitis-linked genes could be used as markers for many other diseases. Moreover, the Bioinformatics tools applied in the current study might be helpful in screening the genes involved in one disease and their association with other diseases as well.

scholarly journals Discoidin Domain Receptor 2 regulates AT1 receptor expression in Angiotensin II-stimulated cardiac fibroblasts via fibronectin-dependent Integrin-β1 signalling

2021 ◽  
Author(s):  
Allen Sam Titus ◽  
Harikrishnan V ◽  
Mingyi Wang ◽  
Edward G Lakkatta ◽  
Shivakumar Kailasam
Keyword(s):  
Angiotensin Ii ◽  
Collagen Type ◽  
Cardiac Fibroblasts ◽  
Collagen Type I ◽  
Cardiac Fibroblast ◽  
Regulatory Role ◽  
Type I ◽  
Integrin Β1 ◽  
Fibronectin Expression

Fibronectin is an extracellular matrix glycoprotein with a regulatory role in fundamental cellular processes. Recent reports on the cardioprotective effect of fibronectin inhibition in a setting of myocardial injury suggest a role for fibronectin in cardiac fibroblast function, which remains largely unexplored. This study probed the molecular basis and functional implications of fibronectin gene expression in cardiac fibroblasts exposed to Angiotensin II, a potent pro-fibrotic factor in the myocardium. Using gene knockdown and over-expression approaches, western blotting and promoter pull-down assay, we show that collagen type I-activated Discoidin Domain Receptor 2 (DDR2) mediates Angiotensin II-stimulated transcriptional up-regulation of fibronectin expression by Yes-activated Protein in cardiac fibroblasts. Further, siRNA-mediated fibronectin knockdown attenuated Angiotensin II-dependent expression of anti-apoptotic cIAP2 and promoted cell death under oxidative stress. Fibronectin was also found to mediate Angiotensin II-stimulated collagen type I expression. Importantly, an obligate role for fibronectin was observed in Angiotensin II-stimulated expression of its receptor, AT1R, which would link ECM signalling and Angiotensin II signalling in cardiac fibroblasts. Moreover, the regulatory role of DDR2-dependent fibronectin expression in Ang II-stimulated cIAP2, collagen type I and AT1R expression was mediated by Integrin-β1-integrin-linked kinase signalling. The pro-survival role of fibronectin in cardiac fibroblasts and its regulatory role in collagen and AT1R expression, downstream of DDR2, could be critical determinants of cardiac fibroblast-mediated wound healing following myocardial injury. Our findings point to a complex mechanism of regulation of cardiac fibroblast function involving two major extracellular matrix proteins, collagen type I and fibronectin, and their receptors, DDR2 and Integrin-β1.

Nicotine Induces Collagen Type I Expression In Lung: Role Of Fibroblasts And Implications For Tobacco-Related Inflammation

2011 ◽  
Author(s):  
Glenn W. Vicary ◽  
Edilson Torres-Gonzalez ◽  
Tanmay S. Panchabhai ◽  
Jeffrey D. Ritzenthaler ◽  
Jesse Roman
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Type I

scholarly journals The “central vein sign” in inflammatory demyelination: The role of fibrillar collagen type I

2019 ◽  
Vol 85 (6) ◽  
pp. 934-942 ◽  
Author(s):  
Martina Absinta ◽  
Govind Nair ◽  
Maria Chiara G. Monaco ◽  
Dragan Maric ◽  
Nathanael J. Lee ◽  
...  
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Central Vein ◽  
Type I ◽  
Fibrillar Collagen

scholarly journals Immunohistochemical distribution of collagens types IV, V, and VI and of pro-collagens types I and III in human alveolar bone and dentine.

1986 ◽  
Vol 34 (11) ◽  
pp. 1417-1429 ◽  
Author(s):  
J Becker ◽  
D Schuppan ◽  
H Benzian ◽  
T Bals ◽  
E G Hahn ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Collagen Type ◽  
Alveolar Bone ◽  
Organic Matrix ◽  
Collagen Type I ◽  
Basement Membranes ◽  
Type I ◽  
Collagen Type Iii ◽  
Type Iii ◽  
Hard Tissues

The aim of the present study was to characterize the composition of the organic matrix in alveolar jaw bone and dentine using antibodies against pro-collagens Types I and III and collagens Types IV, V, and VI. After demineralization of oral hard tissues in 0.2 N HCl, antigenicity was well preserved and the distribution of the pro-collagens and collagens could be demonstrated. Staining for pro-collagen Type I was prominent around osteoblasts and in pre-dentine, indicating active de novo synthesis of Type I pro-collagen. Pro-collagen Type I was ubiquitous but was less abundant in bone and dentine, whereas pro-collagen Type III was seen only in areas of bone remodeling, in peritubular spaces, and in pre-dentine. Type IV collagen was limited to the basement membranes of vessels in osteons and bone marrow. Type V collagen was detected neither in pre-dentine nor in bone. In contrast, Type VI collagen was found in dentine and bone, showing a faint but homogeneous staining which, similarly to pro-collagen Type III, was pronounced around osteoblasts and in pre-dentine, areas of active bone and dentine formation. This study showed that the organic matrix of dentine and bone contains Type VI as well as Type I collagen. Pro-collagen Type III (and to a lesser extent collagen Type VI) is transiently produced during new formation and remodeling of oral hard tissues, and disappears once the matrix calcifies. Type I pro-collagen qualifies as a general marker protein for increased osteoblastic activity. We conclude that immunostaining for the different collagen/pro-collagen types can be used to assess normal or abnormal stages of bone/dentine formation.

Sign in / Sign up

Export Citation Format

Share Document